Heart circulation

Chapter 13

Heart and Circulation

Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Functions of the Circulatory
System
 Transportation:
 Respiratory:
 Transport 02 and C02.
 Nutritive:
 Carry absorbed digestion products to liver and
to tissues.
 Excretory:
 Carry metabolic wastes to kidneys to be
excreted.


Functions of the Circulatory
System (continued)

 Regulation:
 Hormonal:
 Carry hormones to target tissues to produce
their effects.
 Temperature:
 Divert blood to cool or warm the body.
 Protection:
 Blood clotting.
 Immune:
 Leukocytes, cytokines and complement act
against pathogens.


Components of Circulatory
System

 Cardiovascular System (CV):
 Heart:
 Pumping action creates pressure head needed to push blood
through vessels.
 Blood vessels:
 Permits blood flow from heart to cells and back to the heart.
 Arteries, arterioles, capillaries, venules, veins.

 Lymphatic System:
 Lymphatic vessels transport interstitial fluid.
 Lymph nodes cleanse lymph prior to return in venous blood.


Composition of Blood
 Plasma:
 Straw-colored liquid.
 Consists of H20 and dissolved solutes.
 Ions, metabolites, hormones, antibodies.
 Na+ is the major solute of the plasma.

 Plasma proteins:
 Constitute 7-9% of plasma.
 Albumin:
 Accounts for 60-80% of plasma proteins.
 Provides the colloid osmotic pressure needed to
draw H20 from interstitial fluid to capillaries.
 Maintains blood pressure.


Composition of the Blood (continued)

 Plasma proteins (continued):
 Globulins:
 α globulin:
 Transport lipids and fat soluble vitamins.
 β globulin:
 Transport lipids and fat soluble vitamins.
 γ globulin:
 Antibodies that function in immunity.
 Fibrinogen:
 Constitutes 4% of plasma proteins.
 Important clotting factor.
 Converted into fibrin during the clotting process.


Composition of the Blood (continued)

 Serum:
 Fluid from clotted blood.
 Does not contain fibrinogen.
 Plasma volume:
 Number of regulatory mechanisms in the
body maintain homeostasis of plasma
volume.
 Osmoreceptors.
 ADH.
 Renin-angiotensin-aldosterone system.


Erythrocytes

 Flattened biconcave discs.
 Provide increased surface area through which
gas can diffuse.
 Lack nuclei and mitochondria.
 Half-life ~ 120 days.
 Each RBC contains 280 million hemoglobin
with 4 heme chains (contain iron).
 Removed from circulation by phagocytic cells
in liver, spleen, and bone marrow.


Leukocytes
 Contain nuclei and mitochondria.
 Move in amoeboid fashion.
 Can squeeze through capillary walls (diapedesis).
 Almost invisible, so named after their staining
properties.
 Granular leukocytes:
 Help detoxify foreign substances.
 Release heparin.
 Agranular leukocytes:
 Phagocytic.
 Produce antibodies.


Platelets (thrombocytes)
 Smallest of formed elements.
 Are fragments of megakaryocytes.
 Lack nuclei.
 Capable of amoeboid movement.
 Important in blood clotting:
 Constitute most of the mass of the clot.
 Release serotonin to vasoconstrict and reduce
blood flow to area.
 Secrete growth factors:
 Maintain the integrity of blood vessel wall.
 Survive 5-9 days.


Blood Cells and Platelets


Hematopoiesis
 Undifferentiated cells gradually differentiate to
become stem cells, that form blood cells.
 Occurs in myeloid tissue (bone marrow of long
bones) and lymphoid tissue.
 2 types of hematopoiesis:
 Erythropoiesis:
 Formation of RBCs.
 Leukopoiesis:
 Formation of WBCs.


Erythropoiesis
 Active process.
 2.5 million RBCs are produced every second.
 Primary regulator is erythropoietin.
 Binds to membrane receptors of cells that will become erythroblasts.
 Erythroblasts transform into normoblasts.
 Normoblasts lose their nuclei to become reticulocytes.
 Reticulocytes change into mature RBCs.
 Stimulates cell division.
 Old RBCs are destroyed in spleen and liver.
 Iron recycled back to myeloid tissue to be reused in hemoglobin
production.
 Need iron, vitamin B12 and folic acid for synthesis.


Leukopoiesis
 Cytokines stimulate different types and stages of WBC
production.
 Multipotent growth factor-1, interleukin-1, and
interleukin-3:
 Stimulate development of different types of WBC

cells.
 Granulocyte-colony stimulating factor (G-CSF):
 Stimulates development of neutrophils.

 Granulocyte-monocyte colony stimulating factor (GM-
CSF):
 Simulates development of monocytes and

eosinophils.


RBC Antigens and Blood Typing
 Each person’s blood type determines which
antigens are present on their RBC surface.
 Major group of antigens of RBCs is the ABO
system:
 Type A:  Type AB:
Only A antigens Both A and B
present. antigens present.
 Type B:  Type O:
Only B antigens Neither A or B
present. antigens present.


RBC Antigens and Blood Typing
(continued)

 Each person inherits 2 genes that
control the production of ABO groups.
 Type A:  Type AB:
May have inherited A gene from Inherited the A gene from one
each parent. parent and the B gene from the
May have inherited A gene from one other parent.
parent and O gene from the other.
 Type O:
 Type B: Inherited O gene from each
parent.
May have inherited B gene from
each parent.
May have inherited B gene from one

parent and O gene from the other
parent.


Transfusion Reactions

If blood types do not match,
Insert fig. 13.6


the recipient’s antibodies
attach to donor’s RBCs and
agglutinate.
 Type O:
 Universal donor:
 Lack A and B antigens.
 Recipient’s antibodies
cannot agglutinate the
donor’s RBCs.
 Type AB:
 Universal recipient:
 Lack the anti-A and anti-B
antibodies.
 Cannot agglutinate donor’s
RBCs.


Rh Factor
 Another group of antigens found on RBCs.
 Rh positive:
 Has Rho(D) antigens.
 Rh negative:
 Does not have Rho(D) antigens.
 Significant when Rh- mother gives birth to Rh+ baby.
 At birth, mother may become exposed to Rh+ blood of fetus.
 Mother at subsequent pregnancies may produce antibodies
against the Rh factor.
 Erythroblastosis fetalis:
 Rh- mother produces antibodies, which cross placenta.
 Hemolysis of Rh+ RBCs in the fetus.


Blood Clotting

 Function of platelets:
 Platelets normally repelled away from
endothelial lining by prostacyclin
(prostaglandin).
 Do not want to clot normal vessels.
 Damage to the endothelium wall:
 Exposes subendothelial tissue to the blood.


Blood Clotting (continued)

 Platelet release reaction:
 Endothelial cells secrete von Willebrand factor to cause
platelets to adhere to collagen.
 When platelets stick to collagen, they degranulate as
platelet secretory granules:
 Release ADP, serotonin and thromboxane A2.
 Serotonin and thromboxane A2 stimulate vasoconstriction.
 ADP and thromboxane A2 make other platelets “sticky.”
 Platelets adhere to collagen.

 Stimulates the platelet release reaction.

 Produce platelet plug.
 Strengthened by activation of plasma clotting factors.



 Platelet plug strengthened by fibrin.
 Clot reaction:
 Contraction of the platelet mass forms a more
compact plug.
 Conversion of fibrinogen to fibrin occurs.
 Conversion of fibrinogen to fibrin:
 Intrinsic Pathway:
 Initiated by exposure of blood to a negatively charged
surface (collagen).
 This activates factor XII (protease), which activates other
clotting factors.
 Ca2+ and phospholipids convert prothrombin to thrombin.
 Thrombin converts fibrinogen to fibrin.
 Produces meshwork of insoluble fibrin polymers.



 Extrinsic pathway:
 Thromboplastin is not a part of the blood,
so called extrinsic pathway.
 Damaged tissue releases thromboplastin.
 Thromboplastin initiates a short cut to formation
of fibrin.


Dissolution of Clots

 Activated factor XII converts an inactive
molecule into the active form (kallikrein).
 Kallikrein converts plasminogen to plasmin.
 Plasmin is an enzyme that digests the fibrin.
 Clot dissolution occurs.
 Anticoagulants:
 Heparin:
 Activates antithrombin III.
 Coumarin:
 Inhibits cellular activation of vitamin K.


Acid-Base Balance in the Blood

 Blood pH is maintained within a narrow
range by lungs and kidneys.
 Normal pH of blood is 7.35 to 7.45.
 Some H+ is derived from carbonic acid.
 H20 + C02 H2C03 H+ + HC03-


Acid-Base Balance in the Blood
(continued)

 Types of acids in the body:
 Volatile acids:
 Can leave solution and enter the atmosphere as
a gas.
 Carbonic acid.
H20 + C02 H2C03 H+ + HC03-
 Nonvolatile acids:
 Acids that do not leave solution.
 Byproducts of aerobic metabolism, during anaerobic
metabolism and during starvation.
 Sulfuric and phosphoric acid.


Buffer Systems

 Provide or remove H+ and stabilize the
pH.
 Include weak acids that can donate H+
and weak bases that can absorb H+.
 HC03- is the major buffer in the plasma.
 H+ + HC03- H2C03
 Under normal conditions excessive H+ is
eliminated in the urine.


Acid Base Disorders

 Respiratory acidosis:  Metabolic acidosis:
 Hypoventilation.  Gain of fixed acid or loss
 Accumulation of CO2. of HCO3-.
 pH decreases.  Plasma HCO3- decreases.
pH decreases.
Respiratory



alkalosis:  Metabolic alkalosis:
 Hyperventilation.
 Loss of fixed acid or gain
 Excessive loss of CO2. of HCO3-.
 pH increases.  Plasma HCO3- increases.
 pH increases.


pH

 Normal pH is obtained when the ratio of
HCO3- to C02 is 20:1.
 Henderson-Hasselbalch equation:
 pH = 6.1 + log = [HCO3-]

[0.03PC02]


Pulmonary and Systemic
Circulations
 Pulmonary circulation:
 Path of blood from right
ventricle through the
lungs and back to the
heart.
 Systemic circulation:
 Oxygen-rich blood
pumped to all organ
systems to supply
nutrients.
 Rate of blood flow
through systemic
circulation = flow rate
through pulmonary
circulation.


Atrioventricular and Semilunar
Valves
 Atria and ventricles are separated into 2 functional
units by a sheet of connective tissue by AV
(atrioventricular) valves.
 One way valves.
 Allow blood to flow from atria into the ventricles.
 At the origin of the pulmonary artery and aorta are
semilunar valves.
 One way valves.
 Open during ventricular contraction.
 Opening and closing of valves occur as a result of
pressure differences.


Atrioventricular and Semilunar
Valves


Cardiac Cycle
 Refers to the repeating pattern of contraction
and relaxation of the heart.
 Systole:
 Phase of contraction.

 Diastole:
 Phase of relaxation.

 End-diastolic volume (EDV):
 Total volume of blood in the ventricles at the end of
diastole.
 Stroke volume (SV):
 Amount of blood ejected from ventricles during systole.
 End-systolic volume (ESV):
 Amount of blood left in the ventricles at the end of
systole.


Cardiac Cycle (continued)

 Step 1: Isovolumetric contraction:
 QRS just occurred.
 Contraction of the ventricle causes ventricular pressure to
rise above atrial pressure.
 AV valves close.
 Ventricular pressure is less than aortic pressure.
 Semilunar valves are closed.
 Volume of blood in ventricle is EDV.
 Step 2: Ejection:
 Contraction of the ventricle causes ventricular pressure to
rise above aortic pressure.
 Semilunar valves open.
 Ventricular pressure is greater than atrial pressure.
 AV valves are closed.
 Volume of blood ejected: SV.



 Step 3: T wave occurs:
 Ventricular pressure drops below aortic pressure.
 Step 4: Isovolumetric relaxation:
 Back pressure causes semilunar valves to close.
 AV valves are still closed.
 Volume of blood in the ventricle: ESV.
 Step 5: Rapid filling of ventricles:
 Ventricular pressure decreases below atrial pressure.
 AV valves open.
 Rapid ventricular filling occurs.



 Step 6: Atrial
systole:
 P wave occurs.
 Atrial contraction.
 Push 10-30% more
blood into the
ventricle.


Heart Sounds

 Closing of the AV and
semilunar valves.
 Lub (first sound):
 Produced by closing of the
AV valves during
isovolumetric contraction.
 Dub (second sound):
 Produced by closing of the
semilunar valves when
pressure in the ventricles
falls below pressure in the
arteries.


Heart Murmurs
 Abnormal heart sounds produced by abnormal patterns
of blood flow in the heart.
 Defective heart valves:
 Valves become damaged by antibodies made in response to
an infection, or congenital defects.
 Mitral stenosis:
 Mitral valve becomes thickened and calcified.
 Impairs blood flow from left atrium to left ventricle.
 Accumulation of blood in left ventricle may cause pulmonary HTN.
 Incompetent valves:
 Damage to papillary muscles.
 Valves do not close properly.
 Murmurs produced as blood regurgitates through valve flaps.


Heart Murmurs

 Septal defects:
 Usually congenital.
 Holes in septum
between the left
and right sides of
the heart.
 May occur either in
interatrial or
interventricular
septum.
 Blood passes from
left to right.


Electrical Activity of the Heart
 SA node:
 Demonstrates
automaticity:
 Functions as the
pacemaker.
 Spontaneous
depolarization
(pacemaker potential):
 Spontaneous diffusion
caused by diffusion of
Ca2+ through slow Ca2+
channels.
 Cells do not maintain a
stable RMP.


Pacemaker AP
 Depolarization:
 VG fast Ca2+ channels open.
 Ca2+ diffuses inward.
 Opening of VG Na+ channels may also contribute
to the upshoot phase of the AP.
 Repolarization:
 VG K+ channels open.
 K+ diffuses outward.
 Ectopic pacemaker:
 Pacemaker other than SA node:
 If APs from SA node are prevented from reaching these
areas, these cells will generate pacemaker potentials.


Myocardial APs
 Majority of myocardial cells have a RMP of –90
mV.
 SA node spreads APs to myocardial cells.
 When myocardial cell reaches threshold, these cells
depolarize.
 Rapid upshoot occurs:
 VG Na+ channels open.
 Inward diffusion of Na+.
 Plateau phase:
 Rapid reversal in membrane polarity to –15 mV.
 VG slow Ca2+ channels open.
 Slow inward flow of Ca2+ balances outflow of K+.


Myocardial APs (continued)

 Rapid repolarization:
 VG K+ channels

open.
 Rapid outward

diffusion of K+.


Conducting Tissues of the Heart

 APs spread through myocardial cells through gap
junctions.
 Impulses cannot spread to ventricles directly
because of fibrous tissue.
 Conduction pathway:
 SA node.
 AV node.
 Bundle of His.
 Purkinje fibers.
 Stimulation of Purkinje fibers cause both
ventricles to contract simultaneously.


Conducting Tissues of the Heart
(continued)


Conduction of Impulse
 APs from SA node spread quickly at rate of
0.8 - 1.0 m/sec.
 Time delay occurs as impulses pass through
AV node.
 Slow conduction of 0.03 – 0.05 m/sec.
 Impulse conduction increases as spread to
Purkinje fibers at a velocity of 5.0 m/sec.
 Ventricular contraction begins 0.1–0.2 sec. after
contraction of the atria.


Refractory Periods
 Heart contracts as
syncytium.
 Contraction lasts
almost 300 msec.
 Refractory periods
last almost as long
as contraction.
 Myocardial muscle
cannot be
stimulated to
contract again until
it has relaxed.
 Summation cannot
occur.


Excitation-Contraction Coupling
in Heart Muscle

 Depolarization of myocardial cell stimulates
opening of VG Ca2+ channels in sarcolema.
 Ca2+ diffuses down gradient into cell.
 Stimulates opening of Ca2+-release channels in SR.
 Ca2+ binds to troponin and stimulates contraction
(same mechanisms as in skeletal muscle).
 During repolarization Ca2+ actively transported
out of the cell via a Na+-Ca2+- exchanger.


Electrocardiogram (ECG/EKG)

 The body is a good conductor of electricity.
 Tissue fluids have a high [ions] that move in
response to potential differences.
 Electrocardiogram:
 Measure of the electrical activity of the heart
per unit time.
 Potential differences generated by heart are conducted
to body surface where they can be recorded on
electrodes on the skin.
 Does NOT measure the flow of blood through
the heart.


ECG Leads
 Bipolar leads:
 Record voltage between
electrodes placed on wrists
and legs.
 Right leg is ground.
 Unipolar leads:
 Voltage is recorded between
a single “exploratory
electrode” placed on body
and an electrode built into
the electrocardiograph.
 Placed on right arm, left arm,
left leg, and chest.
 Allow to view the changing
pattern of electrical activity
from different perspectives.


ECG
 P wave:
 Atrial
depolarization.
 QRS complex:

 Ventricular
depolarization.
 Atrial
repolarization.
 T wave:
 Ventricular


Correlation of ECG with Heart
Sounds
 First heart sound:
 Produced immediately
after QRS wave.
 Rise of intraventricular
pressure causes AV
valves to close.
 Second heart sound:
 Produced after T wave
begins.
 Fall in intraventricular
pressure causes
semilunar valves to
close.


Systemic Circulation

 Arteries.  Role is to direct
 Arterioles. the flow of
blood from the
 Capillaries.
heart to the
 Venules. capillaries, and
 Veins. back to the
heart.


Blood Vessels

 Walls composed of 3 “tunics:”
 Tunica externa:
 Outer layer comprised of connective tissue.
 Tunica media:
 Middle layer composed of smooth muscle.
 Tunica interna:
 Innermost simple squamous endothelium.
 Basement membrane.
 Layer of elastin.


Blood Vessels (continued)

 Elastic arteries:
 Numerous layers of elastin fibers between smooth
muscle.
 Expand when the pressure of the blood rises.
 Act as recoil system when ventricles relax.
 Muscular arteries:
 Are less elastic and have a thicker layer of smooth
muscle.
 Diameter changes slightly as BP raises and falls.
 Arterioles:
 Contain highest % smooth muscle.
 Greatest pressure drop.
 Greatest resistance to flow.


Blood Vessels (continued)

 Most of the blood volume is contained in the
venous system.
 Venules:
 Formed when capillaries unite.
 Very porous.
 Veins:
 Contain little smooth muscle or elastin.
 Capacitance vessels (blood reservoirs).
 Contain 1-way valves that ensure blood flow to the heart.
 Skeletal muscle pump and contraction of
diaphragm:
 Aid in venous blood return of blood to the heart.


Types of Capillaries
 Capillaries:
 Smallest blood vessels.
 1 endothelial cell thick.
 Provide direct access to cells.
 Permits exchange of nutrients and wastes.
 Continuous:
 Adjacent endothelial cells tightly joined together.
 Intercellular channels that permit passage of molecules (other than
proteins) between capillary blood and tissue fluid.
 Muscle, lungs, and adipose tissue.
 Fenestrated:
 Wide intercellular pores.
 Provides greater permeability.
 Kidneys, endocrine glands, and intestines.
 Discontinuous (sinusoidal):
 Have large, leaky capillaries.
 Liver, spleen, and bone marrow.


Atherosclerosis

 Most common form of arteriosclerosis
(hardening of the arteries).
 Mechanism of plaque production:
 Begins as a result of damage to endothelial cell
wall.
 HTN, smoking, high cholesterol, and diabetes.
 Cytokines are secreted by endothelium; platelets,
macrophages, and lymphocytes.
 Attract more monocytes and lymphocytes.


Atherosclerosis (continued)

 Monocytes become
macrophages.
 Engulf lipids and
transform into
foam cells.
 Smooth muscle
cells synthesize
connective tissue
proteins.
 Smooth muscle
cells migrate to
tunica interna, and
proliferate forming
fibrous plaques.


Cholesterol and Plasma
Lipoproteins
 High blood cholesterol associated with
risk of atherosclerosis.
 Lipids are carried in the blood attached
to protein carriers.
 Cholesterol is carried to the arteries by
LDLs (low-density lipoproteins).
 LDLs are produced in the liver.
 LDLs are small protein-coated droplets of
cholesterol, neutral fat, free fatty acids, and
phospholipids.


Cholesterol and Plasma
Lipoproteins (continued)

 Cells in various organs contain receptors for
proteins in LDL.
 LDL protein attaches to receptors.
 The cell engulfs the LDL and utilizes cholesterol for
different purposes.
 LDL is oxidized and contributes to:
 Endothelial cell injury.
 Migration of monocytes and lymphocytes to tunica
interna.
 Conversion of monocytes to macrophages.
 Excessive cholesterol is released from the cells.
 Travel in the blood as HDLs (high-density lipoproteins),
and removed by the liver.
 Artery walls do not have receptors for HDL.


Ischemic Heart Disease
 Ischemia:
 Oxygen supply to tissue
is deficient.
 Most common cause is
atherosclerosis of
coronary arteries.
 Increased [lactic acid]
produced by anaerobic
respiration.
 Angina pectoris:
 Substernal pain.
 Myocardial infarction
(MI):
 Changes in T segment of
ECG.
 Increased CPK and LDH.


Arrhythmias Detected on ECG
 Arrhythmias:
 Abnormal heart rhythms.
 Flutter:
 Extremely rapid rates of
excitation and contraction of
atria or ventricles.
 Atrial flutter degenerates
into atrial fibrillation.
 Fibrillation:
 Contractions of different
groups of myocardial cells at
different times.
 Coordination of pumping
impossible.
 Ventricular fibrillation is
life-threatening.


(continued)

 Bradycardia:
 HR slower < 60 beats/min.
 Tachycardia:
 HR > 100 beats/min.
 First–degree AV nodal block:
 Rate of impulse conduction through AV node
exceeds 0.2 sec.
 P-R interval.
 Second-degree AV nodal block:
 AV node is damaged so that only 1 out of 2-4
atrial APs can pass to the ventricles.
 P wave without QRS.


(continued)

 Third-degree
(complete) AV nodal
block:
 None of the atrial
waves can pass
through the AV
node.
 Ventricles paced by
ectopic pacemaker.


Lymphatic System

 3 basic functions:
 Transports interstitial (tissue) fluid back to
the blood.
 Transports absorbed fat from small
intestine to the blood.
 Helps provide immunological defenses
against pathogens.


Lymphatic System (continued)

 Lymphatic capillaries:
 Closed-end tubules that
form vast networks in
intercellular spaces.
 Lymph:
 Fluid that enters the
lymphatic capillaries.
 Lymph carried from
lymph capillaries, to
lymph ducts, and then
to lymph nodes.
 Lymph nodes filter the
lymph before returning it
to the veins.

Heart circulation

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